Abstract
Cortisol stimulated tyrosine aminotransferase activity (TAT) in fetal rat liver explants in organ culture only if the explants were subjected to a preliminary incubation. The effect was not due to loss of diffusible inhibitors or gain of a diffusible stimulator. In freshly isolated explants, 75% of added cortisol was accounted for after 5 hr as unconjugated tetrahydrocortisol and allo-tetrahydrocortisol. Other metabolites were also formed in small amounts. In explants subjected to preliminary incubation, 80% of the cortisol was recovered unaltered; the remainder appeared as tetrahydro metabolites. These observations are consistent with the hypothesis that maintenance of unaltered intracellular cortisol is essential for TAT induction, and that rapid inactivation of cortisol by the fetal liver retards the response of the tissue to the hormone. (Endocrinology 95: 466, 1974)
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